Hemolytic Uremic Syndrome in Pregnancy and Postpartum

Bruel, Alexandra; Kavanagh, David; Noris, Marina; Delmas, Yahsou; Wong, Edwin K.S.; Bresin, Elena; François, Patrice; Brocklebank, Vicky; Mele, Caterina; Remuzzi, Giuseppe; Loirat, Chantal; Frémeaux‐Bacchi, Véronique; Fakhouri, Fádi

doi:10.2215/cjn.00280117

Cited by 165 publications

(229 citation statements)

References 51 publications

(33 reference statements)

Supporting

Mentioning

216

Contrasting

Unclassified

Order By: Relevance

“…In around 20% of women with aHUS, the disease onset appears to be triggered by pregnancy, occurring most often in the postpartum period (81,82). Outcomes were historically poor, with 76% developing ESRD despite PE (81).…”

Section: Secondary Tmas Pregnancy-associated Tmamentioning

confidence: 99%

Thrombotic Microangiopathy and the Kidney

Brocklebank

Wood

Kavanagh

2017

CJASN

Self Cite

259

282

View full text Add to dashboard Cite

Thrombotic microangiopathy can manifest in a diverse range of diseases and is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and organ injury, including AKI. It can be associated with significant morbidity and mortality, but a systematic approach to investigation and prompt initiation of supportive management and, in some cases, effective specific treatment can result in good outcomes. This review considers the classification, pathology, epidemiology, characteristics, and pathogenesis of the thrombotic microangiopathies, and outlines a pragmatic approach to diagnosis and management.

show abstract

Section: Secondary Tmas Pregnancy-associated Tmamentioning

confidence: 99%

Thrombotic Microangiopathy and the Kidney

Brocklebank

Wood

Kavanagh

2017

CJASN

Self Cite

259

282

View full text Add to dashboard Cite

show abstract

“…malignant hypertension) is present. Diagnostic and treatment dilemmas frequently arise, exemplified in pregnancy/postpartum, where potential causes of TMA include HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome, severe postpartum haemorrhage, auto‐immune diseases, aHUS and TTP …”

Section: Introductionmentioning

confidence: 99%

Consensus opinion on diagnosis and management of thrombotic microangiopathy in Australia and New Zealand

Fox

Cohney

Kausman

et al. 2018

Internal Medicine Journal

View full text Add to dashboard Cite

Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. Although TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4-8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 (a disintegrin and metalloprotease thrombospondin, number 13) activity. A sodium citrate plasma sample should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin-associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC-HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC-HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. Although early confirmation of aHUS is often not possible, except in the minority of patients in whom auto-antibodies against factor H are identified, genetic testing ultimately reveals a complement-related mutation in a significant proportion of aHUS cases. The presence of other TMA-associated conditions (e.g. infection, pregnancy/postpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.

show abstract

“…malignant hypertension) is present. Diagnostic and treatment dilemmas frequently arise, exemplified in pregnancy/postpartum, where potential causes of TMA include HELLP (haemolysis, elevated liver enzymes, and low platelets) syndrome, severe postpartum haemorrhage, autoimmune diseases, aHUS and TTP …”

mentioning

confidence: 99%

Consensus opinion on diagnosis and management of thrombotic microangiopathy in Australia and New Zealand

et al. 2018

View full text Add to dashboard Cite

Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. While TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4–8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 activity (a disintegrin and metalloprotease thrombospondin, number 13). A sodium citrate plasma sample should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin‐associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC‐HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC‐HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. While early confirmation of aHUS is often not possible, except in the minority of patients in whom autoantibodies against factor H are identified, genetic testing ultimately reveals a complement‐related mutation in a significant proportion of aHUS cases. The presence of other TMA‐associated conditions (e.g. infection, pregnancy/postpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.

show abstract

Hemolytic Uremic Syndrome in Pregnancy and Postpartum

Abstract: Pregnancy-associated hemolytic uremic syndrome and atypical hemolytic uremic syndrome nonrelated to pregnancy have the same severity at onset and during follow-up and the same frequency of complement gene variants.

Cited by 165 publications

References 51 publications

Thrombotic Microangiopathy and the Kidney

Thrombotic Microangiopathy and the Kidney

Consensus opinion on diagnosis and management of thrombotic microangiopathy in Australia and New Zealand

Consensus opinion on diagnosis and management of thrombotic microangiopathy in Australia and New Zealand

Contact Info

Product

Resources

About